Abstract
Objectives
Atypical protein kinase C iota (aPKC-ι) and its associated intracellular molecules, E-cadherin and β-catenin, are important for cell polarization in tumorigenesis and progression. Expression of aPKC-ι, P-aPKC-ι (activated aPKC-ι), E-cadherin, and β-catenin in hepatocellular carcinoma (HCC) was measured, and correlation with clinicopathological characteristics of HCC was analyzed.
Methods
Paraffin-embedded tumor tissue was obtained from patients with HCC after resection without preoperative radiotherapy or chemotherapy. Gene expression was detected by polymerase chain reaction (PCR), and protein expression was detected by immunohistochemistry and Western blot analysis. Expressions of aPKC-ι, P-aPKC-ι, E-cadherin, and β-catenin were analyzed with relation to the clinicopathological data.
Results
The gene and protein expression of aPKC-ι are obviously higher in HCC tissues than that in peritumoral tissues and normal tissues by semiquantitative PCR and immunohistochemistry methods. Accumulation of aPKC-ι in HCC cytoplasm and nucleolus inhibited the later formation of belt-like adherens junctions (AJs) and/or tight junctions (TJs) in cell–cell contact. E-cadherin was reduced and accumulation of cytoplasm β-catenin was increased in HCC. The expression of aPKC-ι was closely related to pathological differentiation, tumor size, invasion, and metastasis of HCC.
Conclusion
Accumulation of cytoplasm aPKC-ι may reflect pathological differentiation, invasion, and metastasis potential of HCC. In this regard, our study on HCC revealed the potential usefulness of aPKC-ι, E-cadherin, and β-catenin as a prognostic marker, closely related to pathological differentiation, invasion, metastasis, and prognosis of HCC.
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Acknowledgement
This work was supported by grant no. 30672040 to Professor Jianming Wang, M.D. from the National Natural Science Foundation of China.
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Du, GS., Wang, JM., Lu, JX. et al. Expression of P-aPKC-ι, E-Cadherin, and β-Catenin Related to Invasion and Metastasis in Hepatocellular Carcinoma. Ann Surg Oncol 16, 1578–1586 (2009). https://doi.org/10.1245/s10434-009-0423-7
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DOI: https://doi.org/10.1245/s10434-009-0423-7